Please use this identifier to cite or link to this item:
|Title:||Negative regulation of β-adrenergic function by hydrogen sulphide in the rat hearts||Authors:||Yong, Q.C.
|Issue Date:||2008||Citation:||Yong, Q.C., Pan, T.-T., Hu, L.-F., Bian, J.-S. (2008). Negative regulation of β-adrenergic function by hydrogen sulphide in the rat hearts. Journal of Molecular and Cellular Cardiology 44 (4) : 701-710. ScholarBank@NUS Repository. https://doi.org/10.1016/j.yjmcc.2008.01.007||Abstract:||β-Adrenoceptor is over-stimulated during myocardial ischemia, in which hydrogen sulphide (H2S) concentration was found to be lowered. The present study attempted to investigate if H2S modulates β-adrenoceptor function and the underlying mechanism. We examined the effect of NaHS (a H2S donor) on myocyte contraction and electrically-induced (EI) intracellular calcium ([Ca2+]i) transients upon β-adrenergic stimulation in rat ventricular myocytes with a video edge tracker method and a spectrofluorometric method using fura-2/AM as a calcium indicator, respectively. We found that isoproterenol (ISO, 10- 9-10- 6 M), a β-adrenoceptor agonist, concentration-dependently increased the twitch amplitude of ventricular myocytes, which was attenuated by NaHS (10- 5-10- 3 M) in a dose-dependent manner. The amplitudes and maximal velocities (± dl/dt) of myocyte twitch and EI-[Ca2+]i transient amplitudes were enhanced by ISO, forskolin (an adenylyl cyclase activator), 8-bromoadenosine-3′,5′-cyclic monophosphate (an activator of protein kinase A) and Bay K-8644 (a selective L-type Ca2+ channel agonist). Administration of NaHS (100 μM) only significantly attenuated the effects of ISO and forskolin. Moreover, NaHS reversed ISO-induced cAMP elevation and forskolin-stimulated adenylyl cyclase activity. In addition, stimulation of β-adrenoceptor by ISO significantly decreased endogenous H2S production in rat ventricular myocytes. In conclusion, H2S may negatively modulate β-adrenoceptor function via inhibiting adenylyl cyclase activity. Impairment of this negative modulation during ischemia may induce cardiac arrhythmias. Our study may provide a novel mechanism for ischemia-induced cardiac injury. © 2008 Elsevier Inc. All rights reserved.||Source Title:||Journal of Molecular and Cellular Cardiology||URI:||http://scholarbank.nus.edu.sg/handle/10635/27219||ISSN:||00222828||DOI:||10.1016/j.yjmcc.2008.01.007|
|Appears in Collections:||Staff Publications|
Show full item record
Files in This Item:
There are no files associated with this item.
checked on Aug 12, 2019
WEB OF SCIENCETM
checked on Aug 12, 2019
checked on Aug 10, 2019
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.